Background: The presence of high-density starry dots around the intracerebral hemorrhage (ICH), which we termed as a satellite sign, is occasionally observed in CT. The relationship between ICH with a satellite sign and its functional outcome has not been identified. This study aimed to determine whether the presence of a satellite sign could be an independent prognostic factor for patients with ICH. Methods: Patients with acute spontaneous ICH were retrospectively identified and their initial CT scans were reviewed. A satellite sign was defined as scattered high-density lesions completely separate from the main hemorrhage in at least the single axial slice. Functional outcome was evaluated using the modified Rankin Scale (mRS) at discharge. Poor functional outcome was defined as mRS scores of 3-6. Univariate and multivariate logistic regression analyses were applied to assess the presence of a satellite sign and its association with poor functional outcome. Results: A total of 241 patients with ICH were enrolled in the study. Of these, 98 (40.7%) had a satellite sign. Patients with a satellite sign had a significantly higher rate of poor functional outcome (95.9%) than those without a satellite sign (55.9%, p < 0.0001). Multivariate logistic regression analysis revealed that higher age (OR 1.06; 95% CI 1.03-1.10; p = 0.00016), large hemorrhage size (OR 1.06; 95% CI 1.03-1.11; p = 0.00015), and ICH with a satellite sign (OR 13.5; 95% CI 4.42-53.4; p < 0.0001) were significantly related to poor outcome. A satellite sign was significantly related with higher systolic blood pressure (p = 0.0014), higher diastolic blood pressure (p = 0.0117), shorter activated partial thromboplastin time (p = 0.0427), higher rate of intraventricular bleeding (p < 0.0001), and larger main hemorrhage (p < 0.0001). Conclusions: The presence of a satellite sign in the initial CT scan is associated with a significantly worse functional outcome in ICH patients.
BackgroundCryptococcal meningoencephalitis (CM) causes cerebral infarction, typically, lacunar infarction in the basal ganglia. However, massive cerebral infarction leading to death is rare and its pathophysiology is unclear. We report a case of CM causing massive cerebellar infarction, which led to cerebral herniation and death.Case presentationA 56-year-old man who suffered from dizziness and gait disturbance for one month was admitted to our hospital and subsequently diagnosed with a cerebellar infarction. He had a past medical history of hepatitis type B virus infection and hepatic failure. Although the findings on magnetic resonance imaging (MRI) imitated an arterial infarction of the posterior inferior cerebellar artery, an accompanying irregular peripheral edema was observed. The ischemic lesion progressed, subsequently exerting a mass effect and leading to impaired consciousness. External and internal decompression surgeries were performed. Cryptococcus neoformans was confirmed in the surgical specimen, and the patient was diagnosed with CM. In addition, venule congestion in the parenchyma was observed with extensive fibrosis and compressed veins in the subarachnoid space. The patient died 26 days after admission. Autopsy revealed that pathological changes were localized in the cerebellum.Conclusion C. neoformans can induce extensive fibrosis of the subarachnoid space, which may compress small veins mechanically inducing venule congestion and massive cerebral infarction. In such cases, the clinical course can be severe and even rapidly fatal. An atypical pattern of infarction on MRI should alert clinicians to the possibility of C. neoformans infection.
Non-convulsive status epilepticus describes the syndrome of unexplained impaired consciousness in critically ill patients. Non-convulsive status epilepticus is very likely to lead to delayed diagnosis and poor outcomes because of the absence of convulsive symptoms. EEG is essential for the diagnosis of non-convulsive status epilepticus to establish the association between periodic discharges and rhythmic delta activity in addition to ictal epileptiform discharges according to the Salzburg criteria. Arterial spin labelling, a type of perfusion MRI, has been applied for rapid and non-invasive evaluation of the ictal state. Ictal cerebral cortical hyperperfusion is the most common finding to demonstrate focal onset seizures. Hyperperfusion of the thalamus on single photon emission computed tomography was found in patients with impaired awareness seizures. We hypothesized that thalamocortical hyperperfusion on arterial spin labelling identifies non-convulsive status epilepticus and such thalamic hyperperfusion specifically associates with periodic/rhythmic discharges producing impaired consciousness without convulsion. We identified 27 patients (17 females; age, 39–91 years) who underwent both arterial spin labelling and EEG within 24 h of suspected non-convulsive status epilepticus. We analysed 28 episodes of suspected non-convulsive status epilepticus and compared hyperperfusion on arterial spin labelling with periodic/rhythmic discharges. We evaluated 21 episodes as a positive diagnosis of non-convulsive status epilepticus according to the Salzburg criteria. We identified periodic discharges in 15 (12 lateralized and 3 bilateral independent) episodes and rhythmic delta activity in 13 (10 lateralized, 1 bilateral independent and 2 generalized) episodes. Arterial spin labelling showed thalamic hyperperfusion in 16 (11 unilateral and 5 bilateral) episodes and cerebral cortical hyperperfusion in 24 (20 unilateral and 4 bilateral) episodes. Thalamic hyperperfusion was significantly associated with non-convulsive status epilepticus (P = 0.0007; sensitivity, 76.2%; specificity, 100%), periodic discharges (P < 0.0001; 93.3%; 84.6%), and rhythmic delta activity (P = 0.0006; 92.3%; 73.3%). Cerebral cortical hyperperfusion was significantly associated with non-convulsive status epilepticus (P = 0.0017; 100%; 57.1%) and periodic discharges (P = 0.0349; 100%; 30.8%), but not with rhythmic delta activity. Thalamocortical hyperperfusion could be a new biomarker of non-convulsive status epilepticus according to the Salzburg criteria in critically ill patients. Specific thalamic hyperexcitability might modulate the periodic discharges and rhythmic delta activity associated with non-convulsive status epilepticus. Impaired consciousness without convulsions could be caused by predominant thalamic hyperperfusion together with cortical hyperperfusion but without ictal epileptiform discharges.
The N100m wave response of the auditory evoked magnetic field originates in the posterior part of the bilateral superior temporal planes for either contra- or ipsilateral ear stimulus. Cortical auditory function was evaluated in 14 patients with temporal lobe tumors using a magnetic resonance (MR) imaging-linked whole-head magnetoencephalography (MEG) system. Before surgery, seven patients had normal N100m latency (within the range of the mean +/- 2 standard deviations of 37 normal volunteers) in both normal hemispheres and in those with lesions, and MR imaging indicated no tumor invasion or edema in the posterior one-third of the superior temporal planes, even when the sylvian fissure was shifted upward due to the mass effect. Seven patients had prolonged N100m latency or absence of N100m in the hemisphere containing the lesion, and the posterior portion of the superior temporal plane was involved by the tumor or perifocal edema. Prolonged N100m latency recovered to the normal range after removal of tumors in two of four patients investigated postoperatively. The MEG system can be used to evaluate cortical auditory function noninvasively before and after surgical treatment of temporal lobe tumors.
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